111 Week 2 Worksheet
111 Week 2 Worksheet
111 Week 2 Worksheet
1.) What is Equilibrium Potential and the Resting Potential? What cellular
components are responsible for establishing the Resting Potential?
Equilibrium Potential is the membrane potential at which two fluxes become equal in
magnitude but opposite in direction, causing no net movement of the ion. Resting Potential
is the membrane potential at which neurons have a potential difference across their plasma
membranes, with the inside of the cell negatively charged with respect to the outside at rest.
The cellular components responsible for establishing the Resting Potential are the uneven
distributions of ions, such as Na+ and K+, between the inside and outside of the cell and the
differences in membrane permeabilities to different ions.
2.) What are the functions of Schwann Cells and oligodendrocytes? Give an example of
a condition arising due to death of oligodendrocytes.
The function of Schwann Cells is to myelinate the axons of the peripheral nervous system
(PNS) neurons. The function of oligodendrocytes is to myelinate the axons of the central
nervous system (CNS) neurons. An example of a condition rising due to death of
oligodendrocytes is multiple sclerosis. Multiple sclerosis is a disease in which the immune
system thinks that the oligodendrocytes are infections and attacks the oligodendrocytes and
their myelin, causing nerve cell damage and therefore signals/messages are unable to get
through as efficiently/get through at all. Multiple sclerosis causes symptoms such as vision
loss, pain, fatigue, and impaired coordination.
3.) Explain what is happening within the neuron at each step each step of the action
potential diagram shown below.
1. Steady resting membrane potential is near K+ equilibrium potential because there
are more open K+ channels than Na+ channels (these K+ channels are leak
channels)
2. A depolarizing stimulus occurs and the initial depolarization stimulates the opening
of some voltage-gated Na+ channels, causing further entry of Na+ that adds to the
local membrane depolarization and leading the local membrane to be brought to
threshold potential.
3. Rapid depolarization of the membrane potential occurs due to the initial
depolarization causing a positive feedback loop—Na+ entry causes depolarization,
which opens more voltage-gated Na+ channels and thus cause more Na+ entry.
4. Membrane potential reaches peak value and stops membrane depolarization as the
Na+ permeability rapidly decreases due to the Na+ channels are inactivated. In
addition, the opening of voltage-gated K+ channels are delayed.
5. Voltage-gated K+ channels open, causing increased K+ flux out of the cell rapidly
and repolarization of the membrane back to a negative potential.
6. Return of the membrane to a negative potential causes Na+ channels to return from
inactivated state to closed state (without opening) and K+ channels to also return to
the closed state but relatively slowly. As a result, after an action potential, K+
membrane permeability remains above resting levels and the membrane is
transiently hyperpolarized.
7. Closure of voltage-gated K+ channels returns the membrane potential to its resting
value.
Electrical synaptic transmissions are faster than chemical synaptic transmissions due to the
electrical synapses directly propagating current from the presynaptic to postsynaptic cell as
they are joined by gap junctions. In chemical synapses, there is a brief synaptic delay
between the arrival of an action potential at a presynaptic terminal and the membrane
potential changes in postsynaptic cells as there is a synaptic cleft in between them. As a
result, you can typically find electrical synapses in systems requiring quick responses while
chemical synapses are found in systems that require less urgent responses.
Electrical synapses are also simpler, smaller, and less abundant than chemical synapses.
Nerve impulses are transmitted as electrical signals in electrical synapses while nerve
impulses are transmitted as chemical signals by means of neurotransmitters.
5.) List the neurotransmitters discussed in class, their effect, function and other
pertinent details. Indicate which are catecholamines.
6.) Name the drugs covered in lecture that alter synaptic transmission. What receptors
do they target, which are agonists, which are antagonists, and what are their effects?